Sunday, March 31, 2024

What happened after the Cath lab was activated for a chest pain patient with this ECG?

Sent by anonymous, written by Pendell Meyers

I received a text with this image and no other information:

What do you think?

I simply texted back:  "Definite posterior OMI." The person I was texting knows implicitly based on our experience together that I mean "Definite posterior OMI, assuming the patient's clinical presentation is consistent with ACS."

The patient was a middle-aged female who had acute chest pain of approximately 6 hours duration. The pain was still active at the time of evaluation.

Queen of Hearts:

You can see that the Queen is most concerned with the ST depression in V2 and V3

The physician activated the cath lab and the patient was transported to the cath lab.

The interventional cardiologist then canceled the activation and returned the patient to the ED without doing an angiogram ("Not a STEMI").

I advised that perhaps posterior leads would help to persuade the interventionalist, since the 2022 ACC recommendations include posterior STEMI as a formal STEMI equivalent, but only officially by 0.5 mm STE in the posterior leads. 

So here is a posterior ECG (unfortunately, I am not sure where exactly the precordial leads are, but suffice to say that at least some of leads V2-V6 are posterior leads):
Limb leads also reversed. Leads V3-V4 are clearly posterior leads and have more than 0.5 mm of STE.

Despite the ACC guidelines for posterior STEMI, the cardiologist again refused to take the patient to the cath lab.

Only when the first troponin (high sens trop I) returned at around 22,000 ng/L did the cardiologist reconsider. 

Angiogram reportedly showed acute thrombotic occlusion of the first obtuse marginal which was stented.

Peak troponin was not recorded. 

The patient survived the hospitalization.

Long term follow up is unavailable.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:


If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

 Learning Points

Posterior STEMI is now a formal STEMI equivalent in USA per the ACC, but they only specify it as STE in posterior leads. They have not yet caught up to the literature we have published showing that ST depression maximal in V1-V4 (without another reason, such as abnormal QRS, etc) is specific for posterior OMI in the setting of ACS symptoms:

Ongoing ischemic symptoms in NSTEMI is already an indication for emergent cath, regardless of the ECG.

Sometimes posterior leads help, and sometimes they falsely reassure. 

See some relevant cases below:

Chest pain with anterior ST depression: look what happens if you use posterior leads.

A woman in her 50s with chest pain and lightheadedness and "anterior subendocardial ischemia"

MY Comment, by KEN GRAUER, MD (4/1/2024):

I couldn’t resist making this figure … Even more impressive than posterior leads — Isn’t this Mirror Test absolutely diagnostic of acute posterior OMI in this patient with CP? 
  • For more on the Mirror Test — Please see My Comment in the September 21, 2022 post in Dr. Smith’s ECG Blog.

  • As per Dr. Meyers above — a definite Posterior OMI ...

Figure-1: Mirror-image of leads V1,2,3 from ECG #1.

Thursday, March 28, 2024

Wide Complex Tachycardia -- VT, SVT, or A Fib with RVR? If SVT, is it AVNRT or AVRT?

A 69 y.o. male with pertinent past medical history including Atrial fibrillation, atrial flutter, cardiomyopathy, Pulmonary Embolism, and hypertension presented to the Emergency Department via ambulance for respiratory distress and tachycardia. 

Per EMS report, patient believes he has been in atrial fibrillation for 5 days, since coming down with flu-like illness with rhinorrhea, productive cough, SOB. Patient is on rivaroxaben, carvedilol, and dofetilide (to suppress atrial fib -- rhythm control).  He states that he maybe missed a dose or two during recent illness. On EMS arrival, patient's oxygen saturation was in the high 80s and improved on 4L O2 via nasal cannula. 

He was noted to have irregular heart rhythm with rates 120-170s. BG 248. 

Bedside ultrasound showed volume depletion and no pulmonary edema.

Here is the prehospital ECG:

First ED ECG

What do you think?

Description: Regular Wide Complex Tachycardia at a rate of about 160.  VT?  SVT with aberrancy?  If SVT, is it AVRT or AVNRT?  It appears too regular to be atrial fib with RVR

I inspected this carefully and it is very regular.  Thus, it really cannot be atrial fibrillation

Is it Ventricular Tachycardia, which is usually a regular rhythm?

Smith opinion: I at first thought this was VT and would have electrically cardioverted.  But I changed my mind after seeing the old ECG (below)

I later sent it to Ken Grauer, who annotated as below with the red Xs:

The "Y" in lead II across the bottom appears to be a PVC.  
Thus is it almost impossible that this is VT, even without the old ECG.  Since it is regular, it must be PSVT (AVNRT or AVRT).    
Thus, adenosine is very likely to work here.


If you want to know more detail (skip if you do not need so much detail), especially if it is AVNRT or AVRT, Ken writes the below, where he also agrees that it cannot be atrial fibrillation:

There are 2 places with this otherwise very regular WCT is “interrupted”. The 1st place ( = X) is kind of bizarre, in that QRS morphology look very similar in leads I,II,III — but a little earlier and narrower (almost like this beat may have occurred during the “supernormal conduction” period ( = a truly RARE phenomenon).

But the 2nd interruption = Y — looks to be a PVC — which is why, even before seeing the prior tracing, I suspected this initial ECG was supraventricular (and not VT).  

Smith: this is because it is almost impossible to have a PVC in the midst of VT

I measured intervals with calipers on my big screen — and other than these 2 interruptions, find the rhythm VERY regular. I don’t see evidence of retrograde atrial activity during the WCT — but usually with the “almost regular AFib rhythms” — you can when you measure pick up some slight differences — so my hunch is that the initial ECG is a REENTRY SVT rhythm, that then breaks down to AFib.

Now you CAN on occasion see PVCs during reentry SVTs that do not convert the SVT. Theoretically  — this can occur with BOTH AVNRT and AVRT. In theory, a PVC is more likely to convert AVRT — because part of the reentry pathway is OUTSIDE of the AV Node (ie, passing thru the AP) — and therefore a PVC would be more likely to “run into” the reentry pathway, and convert the rhythm.

In theory, with AVNRT — the reentry pathway is completely contained WITHIN the AV node — so a PVC would seem LESS likely to convert AVNRT, because it “can’t get to” the reentry pathway that is entirely within the AV node — so my hunch is this initial ECG was AVNRT ________________________

The patient was stable enough to look for a previous ECG.  Here it is:

Slow atrial fibrillation, rate controlled with carvedilol presumably
This shows the same QRS morphology (RBBB + LPFB), proving that the rhythm above is supraventricular, and NOT VT (as suspected by the PVC)

The providers realized it was not VT, but did not recognized it as SVT with RBBB/LPFB.  Instead they diagnosed it as Atrial Fib with RVR.

Thus, they did not give adenosine.

A patient who has atrial fib and is on dofetilde is on a "rhythm control" strategy for AF.  Dofetilide is used for atrial fib rhythm control, not for rate control.

The appropriate management would be to give IV fluids first to restore volume in this patient whom they believed had pneumonia as the initiating factor.  I'm not sure if they started with this, but let's assume that they did.

If you think this is atrial fibrillation with RVR, then because the patient is anticoagularted, one could safely sedate and cardiovert.  Of course, this is NOT atrial fib, but rather PSVT, and so adenosine should work. (Some are now advocating for calcium channel blockers, but that discussion is for another day).

The patient did not want to be electrically cardioverted, so they gave metoprolol.

t = 14 minutes, after giving IV metoprolol

Now there is atrial fibrillation with a much slower rate and PVCs.
Metoprolol can sometimes convert SVT, and sometimes the rhythm can change to atrial fibrillation.

t = 16 minutes

Further Care in the ED:

  1. Patient hemodynamically stable, discussed options with patient, would prefer medications before attempting cardioversion
  2. Patient given metoprolol 5 mg IV with improvement in HR to 110-120s, repeated ~q5 mins x3. Patient also given metoprolol PO 50 mg. 
  3. Mag 2g administered 
  4. Appeared mildly hypovolemic on US, LV function grossly preserved, reports decreased PO intake, given gentle 500 cc bolus
  5. CXR with likely infiltrates vs edema, blood cultures collected, started ceftriaxone and azithromycin
  6. Given patient reports not having taken home meds today, given home dofetilide, coreg and xarelto
  7. Labs notable for mild Acute Kidney Injury (Cr 1.5). pH 7.4. 
  8. CT noncon prelim consistent with pneumonia, final read pending
  9. Patient's HR 110s, respiratory effort improved, reported symptomatic improvement

Later in afternoon

After a brief hospital stay, the patient was discharge, still in atrial fibrillation.

On a visit 2 months later, he was cardioverted.

Tuesday, March 26, 2024

A man in his 50s with shortness of breath

Sent by Tom Fiero, written by Pendell Meyers


A man in his 50s presented with acute shortness of breath. Unfortunately we do not have access to the patients presenting vital signs.

Here is his ECG:

Original image, suboptimal quality

Quality improved with PM Cardio digitization

The ECG is highly suggestive of acute right heart strain, with sinus tachycardia, S1Q3T3, and T wave inversions in anterior and inferior with morphology consistent with acute right heart strain. There is also STE in lead III with reciprocal depression in aVL and I, as well as some subendocardial ischemia pattern with STD in V5-V6 and STE in aVR. Thus, the ECG could be considered similar to Aslanger's pattern (inferior OMI plus SEI pattern). We have seen this pattern in many pts with acute right heart strain on this blog.



The combination of T-wave inversion in V1-V3 and in lead III is very specific for acute pulmonary embolism.  Aslanger's is a combination of acute inferior OMI plus subendocardial ischemia, and due to the ischemia vectors, it has STE only in lead III.  It usually presents with an upright T-wave in both precordial leads and in lead III.  

The ECG in this case has an inverted T-wave in both precordial leads and lead III. 

Moreover, what I call "domed" T-wave inversion in V1-V3 is typical for acute PE and NOT typical of ACS (i.e., Wellens'), presumably because the source of the T-wave inversion is RV strain, not LV ischemia.  Moreover, there is tachycardia. Moreover, T-wave inversion in V1-V3 due to ACS is typically seen in reperfusion states when the patient is symptom free.  So everything about this ECG screams acute PE.

No doubt the patient also had hypoxia with no B-lines, clear lungs on auscultation, and no infiltrate or pulmonary edema on chest X-ray, all of which would shout "Pulmonary embolism".  Unfortunately, we don't have those details.

See 4 examples of Aslanger's pattern here: only one has an inverted T in lead III, but with definite ST elevation and also with upright T-waves in V1-V3.


Queen of Hearts:

Overall Interpretation: Not OMI High Confidence, despite noticing the signal mentioned in III and aVL.

Version 1 of Queen of Hearts does not diagnose any other ECG-identifiable condition besides OMI.  Since then, we have taught her to recognize acute right heart strain.  Thus, later versions may be able to diagnose this acute right heart strain pattern!

Further history also revealed a recent knee surgery, and being off of rivaroxaban for unclear reasons.

Acute pulmonary embolism was confirmed on CT:

The patient did well with treatment.

The Queen of Hearts PM Cardio App is now available in the European Union (CE approved) the App Store and on Google Play.  For Americans, you need to wait for the FDA.  But in the meantime:


If you want this bot to help you make the early diagnosis of OMI and save your patient and his/her myocardium, you can sign up to get an early beta version of the bot here.  It is not yet available, but this is your way to get on the list.

See our other acute right heart strain / pulmonary embolism cases:

A man in his 40s with RUQ abdominal pain

A woman in her 50s with shortness of breath

A crashing patient with an abnormal ECG that you must recognize

A man in his 40s with a highly specific ECG

Chest pain, ST Elevation, and tachycardia in a 40-something woman

Repost: Syncope, Shock, AV block, RBBB, Large RV, "Anterior" ST Elevation in V1-V3

A young woman with altered mental status and hypotension

An elderly woman transferred to you for chest pain, shortness of breath, and positive troponin - does she need the cath lab now?

A 30-something woman with chest pain and h/o pulmonary hypertension due to chronic pulmonary emboli

A 30-something with 8 hours of chest pain and an elevated troponin

Syncope, Shock, AV block, Large RV, "Anterior" ST Elevation....

Dyspnea, Chest pain, Tachypneic, Ill appearing: Bedside Cardiac Echo gives the Diagnosis

31 Year Old Male with RUQ Pain and a History of Pericarditis. Submitted by a Med Student, with Great Commentary on Bias!

Chest pain, SOB, Precordial T-wave inversions, and positive troponin. What is the Diagnosis?

Cardiac Ultrasound may be a surprisingly easy way to help make the diagnosis

Answer: pulmonary embolism. Now another, with ultrasound....

This is a quiz. The ECG is nearly pathognomonic. Answer at bottom.

Chest Pain, SOB, anterior T-wave inversion, positive troponin

Anterior T wave inversion due to Pulmonary Embolism

Collapse, pulse present, ECG shows inferior OMI. Then there is loss of pulses with continued narrow complex on the monitor ("PEA arrest")

What do you suspect from this ECG in this 40-something with SOB and Chest pain?

Sunday, March 24, 2024

Palpitations and presyncope in a 40-something

Written by Magnus Nossen

The below ECG is from a 40 something male with no past relevant medical hx. The patient contacted EMS due to sudden onset chest pain, palpitations and lightheadedness. Symptoms occurred while playing soccer. 

Upon seeing this ECG what is your initial interpretation? What is your next step in the management of this patient? 

The initial ECG in todays case was recorded by EMS and shows a very rapid wide complex tachycardia with a heat rate @ about 245 bpm. This is a very fast arrhythmia and most adult patients even if healthy will likely show signs of hemodynamic compromise (hypotension, chest pain, dyspnea) at such fast heart rates if the arrhythmia persists. Cardioversion should be your next step in the management of this patient. The 12 lead ECG can be scrutinized later. 

The patient was «tolerating» the arrhythmia initially (maintaining BP) and was given iv amiodarone by the paramedics en route to the hospital.

Upon arrival he was diaphoretic and profoundly hypotensive. (SBP in the 60s) Measures for immediate cardioversion were undertaken. While the patient was being administered propofol for sedation, the arrhythmia spontaneously terminated. No shock was delivered. The patient’s blood pressure and condition improved instantly. 

Now it is time to have a closer look at the prehospital ECG. The tracing shows a wide complex tachycardia in which the QRS is completely negative in leads II, III and aVF. In the precordial leads there are QS waves in V1-V4. R/S transition occurs late, between lead V5 and V6. The QRS vector is positive in the lateral leads (I and aVL). The QRS axis is directed superiorly and laterally. In the precordial leads there is «LBBB-like» morphology. Together, the frontal plane axis and QRS morphology point toward origin of the arrhythmia from the apical portion of the right ventricle. 

The initial ECG post conversion (not shown) revealed widespread ST-T wave changes as expected following a sustained very rapid tachycardia. Below is a repeat ECG acquired roughly 15 minutes after cessation of the tachyarrhythmia.  

What do you think about the resting ECG? What abnormalities can you identify in this 12 lead?

Smith: The layout here is the Cabrera format, which uses a clockwise format from upper left (aVL) around to I, -aVR, II, aVF, and III.

The resting ECG is not normal for a 40 something male. The tracing shows atrial fibrillation which is very uncommon in a healthy 40 something old male. The QRS is narrow with slight q waves in an inferolateral distribution. Most striking are the pathologic T wave inversions in the precordial leads extending all the way to V6, and also in II, III, aVF (all these T-wave inversions are typical of RV cardiomyopathy)

You might ask if the T-wave inversion in the precordial leads could be related to the preceding tachycardia. Could they be memory T waves? Or maybe T inversions from demand ischemia? The T waves in the precordial leads simply do not look like memory T waves. Also, usually longer periods of abnormal depolarization is required for memory T wave phenomenon to occur. There was an old ECG on file with similar findings in the early precordial leads. This essentially rules out demand ischemia as a cause. (The old ECG was not recognized as pathologic at the time of recording). T wave inversions are more pronounced in the right precordial leads and there is no good reason for a tachydysrhythmia to give demand ischemia mostly in the RV in a presumably healthy individual.

There are PVCs with a distinctly different axis and morphology as compared to the wide complex tachycardia. (The PVCs in this tracing seem to have an RVOT morphology). 

In summary the wide complex tachycardia and the resting ECG should alert you to right ventricular pathology. I put this ECG through the QoH for digitization purposes and the QoH AI algorithm was not fooled by the ST-T changes in this ECG. The interpretation was not OMI with high confidence.

From the available information, the following diagnoses could conceivably be on the list of differentials

  1. Arrhythmogenic (RV) cardiomyopathy with VT 
  2. RV myocardial scar/ischemia causing VT
  3. Any myocardial disease affecting the RV (e.g. myocarditis/sarcoidosis etc)
  4. Antidromic AVRT with a right sided posterolateral AP
  5. Mahaim fibre mediated tachycardia
  6. RVOT, but RVOT should have an inferior axis, not a superior axis as in this ECG

After the arrhythmia terminated the patient stabilized quickly and a bedside echocardiogram was obtained. The videos below show focused views of the right ventricle. The RV is dilated with decreased systolic performance, there is myocardial thinning and hypokinesis of the large areas of the RV, especially the apical regions and RVOT. RV EF on formal study was 34%. Right ventricular end diastolic volume (RVEDV) was significantly increased. Also noted was hypokinesis involving the LV in a non-coronary pattern. LVEF was preserved.

Below are focused views on the right ventricle (left frame) and RVOT (right frame). The videos show that both the RV and the outflow tract are significantly dilated. The RV myocardium shows regional myocardial thinning and aneurysms. 

Below are still images with red arrows pointing to the dilated basal and apical regions of the RV. Circled in yellow is the midventricular region of the RV which shows less dilatation likely owing to restrain by the moderator band. Blue arrows point toward thinning of the myocardium both in the apical region of the RV and in the RVOT.

Discussion: Putting all of the information together this patient is most likely suffering from arrhythmogenic cardiomyopathy (AC) better known as ARVC. The medical hx is typical, with sudden onset tachydysrhythmia during physical exertion. It is not uncommon for the initial presentation to be sudden cardiac death (SCD). In fact it is one of the leading causes of SCD in people age less than 40 years. Thus it is very important to identify this disorder. AC is a disease in which myocardium is replaced by fibrofatty tissue. This usually and predominantly affects the RV free wall and apical regions, but it can affect the left ventricle as well and this is why arrhythmogenic cardiomyopathy is a more precise name for the disorder than ARVC. 

Smith: The 5 entities I look for on all ECGs for patients with syncope who are asymptomatic on arrival with sinus rhythm and no ischemia is:

1. WPW


3. Brugada

4. Long QT

5. RV cardiomyopathy

The origin of the VT in our case is from the apical portion of the RV. There are signs of RV pathology on the ECG (T wave inversions in V1-V3). I do not see any epsilon waves in the post conversion ECG. T wave inversion extends throughout the precordial leads all the way to V6 signifying involvement also of the left ventricular myocardium. This was consistent with echocardiographic and MRi findings in this case. Atrial fibrillation too has an association with ARVC. 

Diagnosis of AC is based on the family hx, patient hx, electrocardiographic, echocardiographic and radiologic features as well as genetic studies. The diagnostic criteria are complex. Clinical and paraclinical findings are grouped into major and minor criteria. For a definite diagnosis 2 major criteria, 1 major and two minor or 4 minor criteria are required. 

Some information on epsilon waves and late potentials: In ARVC late potentials are thought to be caused by early afterdepolarizations of cells in the (right) ventricle. Their amplitude is often too small to show up on a normal ECG. However, when multiple QRS recordings (typically > 200 consecutive QRS complexes) are averaged, random noise is filtered out and late potentials can show up. Such a recording is called a Signal Averaged ECG (SAECG).

Sometimes late potentials can manifest on the regular ECG as epsilon waves. Although the epsilon wave is considered a major diagnostic criterion for arrhythmogenic cardiomyopathy (AC) its diagnostic value is limited because it is a sign of the later stage of the disease. It would be more appropriate to say that the epsilon wave is a “hallmark” of AC, but is of low diagnostic sensitivity. Although the epsilon wave has high specificity for AC, it can be present in other pathological conditions.

As previously mentioned, epsilon waves are not present in the post conversion ECG. Several ECGs were recorded for the patient in today's case. A few days into the hospital stay the patient’s rhythm spontaneously converted to sinus. Another ECG was recorded. The precordial leads are shown below in 50mm/s. Perhaps there was a difference in filter setting but epsilon waves now seem to be readily appreciable in leads V1-V3.

As there are epsilon waves in this case (major criteria) a pathologic SAECG does not really add any diagnostic value. (See this link for a very good discussion on signal averaged ECG)

Patients with AC should be educated with regards to their condition. Strenuous exercise is not recommended as it is thought to lead to disease progression. Malignant arrhythmias in AC patients tend to occur during physical exertion. Antiarrhythmic treatment with betablocker is mainstay and ICD placement should be considered for all patients with syncope or documented ventricular arrhythmia. The patient in today's case was put on betablocker and was given an implantable cardioverter/defibrillator (ICD). Long term follow up is not available.

Learning points
1) AC is not limited exclusively to the RV although RV involvement is the hallm
ark of the disease. 
2) Physical exercise may hasten disease progression. Strenuous exercise should be avoided.
3) Epsilon waves are highly suggestive of arrhythmogenic cardiomyopathy, but they are not pathognomonic as they can occur in other disease states (e.g. sarcoidosis)
4) AC is a chronic progressive disease. Beta-blocker and ICD are used to reduce arrhythmia incidence and arrhythmia related SCD.
5) Sometimes VT ablation can be performed and in rare cases heart transplantation is required. 

Please see below cases for more on arrhythmogenic cardiomyopathy.

MY Comment, by KEN GRAUER, MD (3/22/2024):
ARVD is not a common entity. It's estimated incidence in the general population is ~1 per 2,500-to-5,000 (Shah et al: StatPearls — 2023). However, among younger adults who die suddenly — ARVC/D (Arrhythmogenic Right Ventricular Cardiomyopathy-Dysplasiamay be the cause in up to 5-10% of cases (with this prevalence range depending on demographics and the geographic area of the group studied).
  • From the above statistic, it should be apparent that while ARVC/D is uncommon (if not rare) in the general population — it clearly is an important entity to consider when a younger adult presents for emergency care because of a malignant ventricular arrhythmia.

  • Dr. Meyers' case in the June 3, 2023 post of Dr. Smith's ECG Blog illustrates how despite the infrequency of ARVD (ie, Dr. Meyers had not previously made this diagnosis de novo despite his extensive ED experience!) — Workup and recognition of ARVD as the cause of the patient's presenting VT episode in this June 3, 2023 case led to probable lifesaving implantation of an AICD in this previously healthy young woman.

Similarly, the previously healthy 40-something man presented by Dr. Nossen in today's case features yet another younger adult for whom recognition of ARVD as the cause of his VT episode — once again led to probable lifesaving ICD implantation.
  • With this as introduction — I add the following to Dr. Nossen's insightful presentation:


Regarding the Initial ECG:
  • The most common cause of sustained VT in a previously healthy younger adult — is idiopathic VT. As we've discussed on a number of occasions in Dr. Smith's ECG Blog (See My Comment and summarizing Table in Figure-2 of the February 14, 2022 post) — the Fascicular VTs and the Outflow Track VTs ( = RVOT VT and LVOT VT) are by far, the most common forms of idiopathic VT.
  • Most of the time — the frontal plane axis and QRS morphology on ECG obtained during the VT episode allow ready recognition if one of the above common forms of idiopathic VT is the cause. On occasion, however — distinction between ARVD vs RVOT VT may not be possible on the basis of a single ECG, because both entities may manifest a LBBB-like pattern in the chest leads in association with an inferior axis in the frontal plane.
  • In addition (as per Dr. Nossen) — given the expanded classification of "ARVD" based on the finding of not only RV, but also potential for LV involvement (ie, AC = Arrhythmogenic Cardiomyopathy) — thBOTTOM Line in 2024, is that ECG features are not sufficiently reliable to be depended on for identification of all cases of AC. As a result, in addition to Echo — virtually all younger adults who present with an episode of sustained VT should undergo Cardiac MRI to rule out a more severe form of underlying cardiac pathology.

  • The above said, the initial ECG in today's case (that I have reproduced in Figure-1) does not resemble any of the common types of idiopathic VT because: i) There is marked QRS widening; ii) The shape of the QRS is amorphous (not resembling any known form of conduction defect); — andiii) There is extreme axis deviation ( = an all negative QRS in each of the inferior leads). KEY Point: Echo and MRI are essential components for evaluation in today's case. This would be true regardless of whether epsilon waves are or are not seen on baseline or subsequent ECGs of the patient.

Figure 1: The initial ECG in today's case.


Additional Thoughts on Epsilon Waves:
Since questions continually arise regarding the recognition of epsilon waves — I thought it useful to excerpt parts of my discussion from the above cited June 3, 2023 post in Dr. Smith's ECG Blog.

Why is it so difficult to pick up epsilon waves on a standard 12-lead ECG?
  • There are several reasons ...  

Reason #1: The Wrong Filter Setting is Used ...
All too often — filter settings are ignored. Different settings are typically used for monitoring when emphasis is placed on rhythm determination vs diagnostic mode, for which the focus is on interpreting 12-lead waveforms. Greater filtering is generally used in monitor mode, with a common setting beting between 0.5 Hz and 40 Hz. Doing so has the advantage of minimizing artifact and baseline wander that may affect rhythm interpretation. In contrast — a broader passband (typically from 0.05 Hz to 150 Hz) is recommended for diagnostic mode, where more accurate ST segment analysis is essential.
  • I've taken Figure-2 from the illustration by GarcĂ­a-Niebla et al (Rev Esp Cardiol 69(4):438, 2016) — to show how selection of a 40 Hz cutoff frequency (that is commonly chosen in clinical practice in an attempt to "improve" tracing appearance) may result in disappearance of fine ECG features such as the epsilon wave, that is only optimally seen in Figure-2 at a cutoff high-pass filter setting of 150 Hz (BLUE arrows).

Figure 2: Illustration of the effect of filter settings on the likelihood of seeing epsilon waves on a standard 12-lead ECG.

Reason #2: The Wrong Lead System is Used ...
I strongly recommend the section by Drs. Buttner and Cadogan in Life-In-The-Fast-Lane on the Fontaine Lead — — as this concise review outlines what to know for optimizing your chance of identifying an epsilon wave in a patient with ARVD on ECG. I highlight below a few KEY points from this LITFL Review:
  • Identification of epsilon waves is potentially a most specific ECG sign of ARVD. These small deflections may be seen as a "blip" or "wiggle" either at the end, or just after the QRS complex. They are best seen in leads V1,V2 — and a bit less well seen in V3,V4.
  • LITFL cites a figure of 23% for the frequency of visualizing epsilon waves on a standard ECG. The filter settings used in association with this figure are not mentioned — so given the tendency of all-too-often selecting a 40 Hz high-pass setting (instead of the optimal 150 Hz setting) — an even lower likelihood of finding epsilon waves might be expected on the ECGs sent our way in search of epsilon waves.
  • In contrast — use of special placement of standard ECG machine electrodes called Fontaine Lead Placement — allowed detection of epsilon waves in up to 75% of patients! Rather than reproducing the user-friendly instructions on the LITFL site — I'll refer interested readers directly to their site — —

  • Finally —There are a variety of potential epsilon wave shapes! These include: i) "Wiggle" waves; ii) Small upward spikes; iii) Small downward spikes; and/oriv) Smooth potential waves at the end of the QRS (which result in prolongation of the QRS in lead V1 exceeding duration of the QRS in lead V3 by ≥25 msec.).

How Large and Well-Defined Can Epsilon Waves Be?
Most of the examples of epsilon waves that I have seen show relatively small deflections. Because notation of filter settings is so commonly omitted from the ECGs sent my way — it's impossible to say how much of an effect suboptimal filter settings may have had on this smaller size of these epsilon wave deflections.
  • In today's case — notation of filter settings was absent. That said — Dr. Nossen's magnified view with RED arrows on one of the subsequent ECGs clearly indicate a prominent epsilon wave deflection (seen best in lead V3).

On occasion — epsilon waves can be large and extremely well defined. The ECG in Figure-3 (taken from THIS CASE) — provides the BEST illustration of epsilon waves that I have seen.
  • The rhythm in Figure-3 is sinus — as evidenced by regular upright in lead II P waves, with a constant and normal PR interval. The QRS complex is wide, with QRS morphology consistent with RBBB/LAHB.
  • Note that there is T wave inversion in the anterior leads, as should be expected with ARVD (albeit the presence of RBBB itself could account for some of this anterior T wave inversion).

  • KEY Point: The reason for the bizarre shape of the QRS complex in lead V1 — is that the QRS in this lead is being prolonged by a huge Epsilon wave (dark BLUE arrow).

  • To assist in looking for Epsilon waves in other leads — I dropped a vertical dark BLUE time-line through the peak of the huge Epsilon wave in lead V1 — extending downward through the long lead II rhythm strip at the bottom of the tracing. Doing so defines the point in the 2 simultaneously-recorded long lead rhythm strips that marks the occurrence of the Epsilon wave.
  • Using this reference point we defined for the Epsilon wave in the long lead II and lead V1 rhythm strips — I then extended upward a vertical light BLUE time-line to highlight the expected location of any Epsilon waves that might be seen in simultaneously-recorded leads I,II,III — aVR,aVL,aVF — and V4,V5,V6.
  • The light BLUE arrow in lead II highlights a surprisingly large negative Epsilon wave that is present in this lead.
  • Following these upward extended light BLUE time-lines — we can see that smaller, but definitely-present negative Epsilon waves are also seen in leads IaVLaVF, and V3-thru-V6.
  • Another positive Epsilon wave is seen in lead aVR. 

Figure 3: Epsilon waves in multiple leads! 

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